Basophils release histamine and eosinophils participate in allergic Th2 immune responses

Allergic diseases involve highly coordinated cellular cascades. In allergic type 2 (Th2) immune responses, basophils and eosinophils function as key cellular players, driving both immediate hypersensitivity and ongoing inflammatory pathways.

Cellular mechanisms of histamine release

• Degranulation dynamics: Basophils store histamine in specialized secretory granules. When an individual basophil is activated, it undergoes classical anaphylactic degranulation, releasing approximately 100% of its stored histamine. In bulk laboratory assays, total histamine release ranges from 10% to 90%, representing the proportion of the cellular population successfully stimulated.
• Intracellular signaling: This process is initiated when allergens crosslink IgE antibodies bound to high-affinity Fc$\epsilon$RI receptors. This triggers Src-family kinases (such as Lyn) to phosphorylate ITAMs, recruiting Spleen Tyrosine Kinase (Syk). Downstream, phospholipase C$\gamma$ (PLC$\gamma$) activation generates inositol 1,4,5-trisphosphate ($\text{IP}_3$), mobilizing calcium ($\text{Ca}^{2+}$) to drive the exocytosis of histamine-rich granules.

Eosinophil dynamics in Th2 polarization

• Recruitment and activation: During Th2 immune responses, Th2 cells and group 2 innate lymphoid cells (ILC2s) secrete IL-5, the dominant cytokine controlling eosinophil maturation, survival, and recruitment. Concurrently, IL-4 and IL-13 stimulate the release of eotaxins (CCL11, CCL24, CCL26) and the expression of VCAM-1, drawing eosinophils into inflamed tissues.
• Regulatory and effector roles: Beyond causing tissue damage through cationic proteins, eosinophils act as non-professional antigen-presenting cells (APCs) via MHC class II expression. By releasing preformed cytokines (IL-4, IL-13, and IL-25), they establish a positive feedback loop that maintains the type 2 immune state and prevents a shift toward neutrophil-rich Th1/Th17 pathways.

Bottom line

• The claim is fully supported by scientific evidence. Basophils release histamine via precise, $\text{Ca}^{2+}$-dependent degranulation pathways, and eosinophils serve as both tissue-damaging effectors and critical upstream orchestrators that maintain Th2 immune polarization.